Paraspinal arteriovenous fistula with perimedullary venous drainage.

A paravertebral presacral posttraumatic arteriovenous fistula drained through the ascending lumbar vein to the epidural plexuses and perimedullary veins. The patient did not have symptoms of myelopathy, only low-back pain and radicular hypoesthesia. The lesion was embolized with a large balloon and clinical symptoms disappeared.

Computed tomographic findings in patients with persistent sacroiliac pain after posterior iliac graft harvesting.

STUDY DESIGN: A retrospective study of 24 sacroiliac joint computed tomographic (CT) scans of patients with persistent donor site pain. OBJECTIVE: To illustrate the computed tomographic findings of sacroiliac joints in patients who underwent posterior iliac bone graft harvesting with subsequent persistent donor site pain. SUMMARY OF BACKGROUND DATA: In a previous study the posterior iliac bone harvesting site was divided into three zones. Zone 1 carried no risk of violation of the synovial part of the sacroiliac joint. In Zones 2 and 3 there was a potential risk of violation to the synovial part of the sacroiliac joint. There is no study in the literature on the effect of violating the different parts of the sacroiliac joint during posterior iliac bone graft harvesting. METHODS: Computed tomographic scans of the sacroiliac joints of 22 patients with persistent pain in 24 sacroiliac joints after posterior iliac bone graft harvesting were retrospectively reviewed. RESULTS: Of the 16 sacroiliac joints with evidence of disruption of the inner table at the ligamentous part, 10 showed mild degenerative changes, and 6 showed moderate changes. Three joints with evidence of disruption of the inner table at the synovial part showed severe degenerative changes. Five joints with no evidence of inner table disruption did not show degenerative changes. CONCLUSION: There is a high prevalence of inner table disruption in patients with persistent sacroiliac joint pain after posterior iliac bone graft harvesting. The computed tomographic scan showed that involvement of the synovial part caused more severe degenerative changes than involvement of the ligamentous part.

Computed tomography findings in patients with sacroiliac pain.

This retrospective study evaluated the diagnostic value of computed tomography in patients with sacroiliac pain. Computed tomography scans of the sacroiliac joints of 62 patients with sacroiliac joint pain were reviewed. The criteria to include the patient in the current study were pain relief after a local injection in the sacroiliac joint under computed tomography guidance, a physical examination consistent with a sacroiliac origin of the pain, and negative magnetic resonance imaging of the lumbar spine. A control group consisted of 50 patients of matched age who had computed tomography scans of the pelvis for a reason other than pelvic or back pain. Computed tomography scans showed one or more findings in 57.5% and 31% of the sacroiliac joints in the symptomatic and the control groups, respectively. The computed tomography scans were negative in 37 (42.5%) symptomatic sacroiliac joints with a positive sacroiliac joint injection test. The sensitivity of computed tomography was 57.5 % and its specificity was 69%. The finding of the current study suggests limited diagnostic value of computed tomography in sacroiliac joint disease because of its low sensitivity and specificity. With clinical suspicion of a sacroiliac origin of pain, intraarticular injection is currently the only means to confirm that diagnosis.

Soluble PECAM-1, but not P-selectin, nor osteonectin identify acute myocardial infarction in patients presenting with chest pain.

We sought to determine plasma levels of platelet/endothelial cell adhesion molecule-1 (PECAM-1), P-selectin, and platelet-derived osteonectin, and prospectively compare these data with the discharge diagnosis in patients presenting with chest pain in a community hospital Emergency Department. Soluble antigens were measured by ELISA in 44 subjects including patients with acute myocardial infarction (AMI) (n = 13), chest pain of noncardiac origin (n = 17), and compared to those of age- and sex-matched healthy controls (n = 14). Elevated soluble PECAM-1 (64.5 +/- 18.3 ng/ml, p = 0.019), but not P-selectin (149.5 +/- 49.8 ng/ml, p = NS), nor osteonectin (549. 5 +/- 159.1 ng/ml, p = NS), occurred in the AMI group as compared to patients with noncardiac chest pain (46.2 +/- 7.5 ng/ml, 118.2 +/- 40.1 ng/ml, and 619.4 +/- 74.4 ng/ml, respectively). Increased plasma PECAM-1 may serve as a useful marker in the early detection of patients with AMI. Larger studies will be necessary to confirm the utility of soluble PECAM-1 in identifying AMI among patients presenting with chest pain.

Effect of coronary thrombolysis on the plasma concentration of osteonectin (SPARC, BM40) in patients with acute myocardial infarction.

Osteonectin is a phosphoglycoprotein exclusively located in bone and platelet alpha-granules. Human platelet-derived osteonectin is released into plasma after thrombin-induced activation. Recognizing the unique distribution of the osteonectin pool, we first sought to investigate whether osteonectin could serve as a sensitive marker of platelet activity, and identify patients with acute myocardial infarction (AMI). The second objective was to define the effects of thrombolytic therapy in these patients on the plasma concentrations of osteonectin at prespecified time points following attempted reperfusion. Osteonectin levels by ELISA were determined in AMI patients before thrombolysis and at 3, 6, 12, and 24 hours thereafter and compared with 12 healthy controls. At baseline, soluble osteonectin plasma levels were similar between controls (447. 7+/-20.6 ng/ml) and AMI patients (425.7+/-43.3 ng/mL; p=NS). A significant increase of the soluble osteonectin was observed at 3 hours after thrombolysis (519.4+/-26.9 ng/mL; p=0.03), and was followed by a decrease to baseline levels at 6 hours after attempted reperfusion. Contrary to expectations, the plasma osteonectin level in our pilot study was not a sensitive marker distinguishing patients with AMI. The early peak of soluble osteonectin at 3 hours after thrombolytic therapy is most likely not related to coronary thrombolysis per se but rather to the phasic changes of platelet activity during myocardial ischemia-reperfusion. The unquestionable platelet origin of this protein and the lack of elevated plasma levels of this alpha-granule constituent, challenge the postulate of uniform platelet activation in AMI patients.

Soluble VCAM-1 and E-selectin, but not ICAM-1 discriminate endothelial injury in patients with documented coronary artery disease.

It has been shown that endothelial cell adhesion molecules play an important role in the development of coronary atherosclerosis and inflammatory disease. We sought to test whether soluble vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin are increased in patients with documented coronary artery disease (CAD). Plasma levels of VCAM-1, ICAM-1 and E-selectin were measured in 40 patients with documented CAD, 20 subjects with angiographically documented normal coronary arteries, and 14 healthy volunteers. Patients with documented CAD exhibited significant elevation of VCAM-1 (535 +/- 227.1 ng/ml, p = 0.0001), E-selectin (69.4 +/- 29.4 ng/ml, p = 0.006), but not ICAM-1 (320.5 +/- 65.1 ng/ml, p = 0.9) concentrations as compared to subjects with normal coronary arteries (252.3 +/- 79.8, 49.7 +/- 22.0 and 311.4 +/- 40.2 ng/ml), and healthy controls (110.0 +/- 17.7, 29.0 +/- 2.0 and 237.5 +/- 46.5 ng/ml), respectively. Soluble markers of endothelial injury are not uniformly increased in patients with documented CAD as compared to those with normal coronary arteries and healthy controls. However, VCAM-1 and E-selectin, but not ICAM-1 could identify endothelial injury in such patients.

The effect of chronic azithromycin therapy on soluble endothelium-derived adhesion molecules in patients with coronary artery disease.

In patients with coronary artery disease (CAD), azithromycin therapy is associated with decreased cytokine levels and overall reduction of inflammation. Chlamydia pneumoniae (C.Pn) is a common pathogen that may be an important factor in the development and progression of atherosclerosis. Cell-adhesion molecules have an important role in recruitment of inflammatory cells during plaque development and are expressed by endothelial cells on activation. We sought to define the effect of treatment with azithromycin on circulating levels of soluble vascular cell-adhesion molecule (VCAM-I), intercellular adhesion molecule (ICAM-1), and E-selectin in patients with CAD. Plasma concentrations of VCAM-1, ICAM-1, and E-selectin were measured in 40 patients with documented CAD and a positive (> or = 1:16) immunoglobulin G (IgG) titer against C.Pn, 20 subjects with normal coronary arteries, and 14 healthy volunteers. Patients were assigned randomly to receive either 500 mg/wk of azithromycin or placebo for 3 months. Serum samples were obtained at baseline, at 3 months, and during the follow-up visit at 6 months. Patients with documented CAD exhibited elevation of VCAM-1 (535 +/- 227 ng/ ml; p = 0.0001) and E-selectin (69 +/- 29 ng/ml; p = 0.006), but not ICAM-1 (321 +/- 65 ng/ml) concentrations as compared with the patients with angiographically proven normal coronary arteries (252 +/- 80; 50 +/- 22; and 311 +/- 40 ng/ml) and healthy controls (110 +/- 18; 29 +/- 2; and 238 +/- 47 ng/ml, respectively). Prolonged treatment with azithromycin did not significantly affect the plasma levels of soluble VCAM-1, ICAM-1, and E-selectin. Soluble markers of endothelial activation are markedly increased in patients with documented CAD as compared with those with normal coronary arteries and healthy controls. Despite substantial heterogeneity in plasma E-selectin, ICAM-1, and VCAM-1 levels, long-term azithromycin treatment did not affect plasma levels of these adhesion molecules, indicative of endothelial activation, over a period of 6 months.